Audiogenic seizure (AGS) models of developmental or genetic origin manifest
characteristic indices of generalized seizures such as clonus or tonus in
rodents. Studies of seizure-resistant strains in which AGS is induced by in
tense sound exposure during postnatal development provide models in which o
ther neural abnormalities are not introduced along with AGS susceptibility.
A critical feature of all AGS models is the reduction of neural activity i
n the auditory pathways from deafness during development. The initiation an
d propagation of AGS activity relies upon hyperexcitability in the auditory
system, particularly the inferior colliculus (IC) where bilateral lesions
abolish AGS. GABAergic and glutaminergic mechanisms play crucial roles in A
GS, as in temporal lobe models of-epilepsy, and participate in AGS modulato
ry and efferent systems including the superior colliculus, substantia nigra
, basal ganglia and structures of the reticular formation. Catecholamine an
d indolamine systems also influence AGS severity. AGS models are useful for
elucidating the underlying mechanisms for formation and expression of gene
ralized epileptic behaviors, and evaluating the efficacy of modern treatmen
t strategies such as anticonvulsant medication and neural grafting. (C) 200
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